Pentraxin PTX3 consists of two structural domains, a N-terminal domain unrelated to any known molecule, and a C-terminal domain similar to that of the short pentraxins such as C-reactive protein (CRP) (Bottazzi et al., J. Biol. Chem. 1997; 272: 32817-32823). A substantial similarity has been found between human PTX3 (hPTX3) and animal PTX3s. To date, the biological function of PTX3 has not yet been fully understood, although PTX3 was the first member of the long pentraxin family to be cloned (Breviario et al., J. Biol. Chem. 1992; 267: 22190-22197).
The carboxyl half-domain of PTX3 aligns with the full-length sequence of CRP and SAP, whereas the NH2-terminal part of the protein does not show any significant homology with other known proteins. PTX3 recognizes and binds structures different from those recognized by CRP and SAP (Mantovani et al., PTX3/TSG6; The Cytokine Handbook in press). In contrast to short pentraxins, PTX3 is produced by various cell types, including endothelial cells, monocytes and macrophages (Vouret-Craviari et al., Infect. Immun. 1997; 65: 1343-1350). mononuclear phagocytes (Vidal Alles et al., Blood 1994; 84: 3483-3493), in response to primary inflammation-mediators such as Interleukin-1 β (IL-1β), tumor necrosis factor α (TNF-α), bacterial products, and others (Basile et al., J. Biol. Chem. 1997; 272: 8172-8178). The inoculation of these molecules in mice induces high levels of PTX3 expression in heart and skeletal muscles (Introna et al., Blood 1996; 87:1862-1872).
Recent studies have demonstrated that PTX3 is increased in patients with acute or chronic inflammatory diseases such as sepsis and myocardial infarction, but no correlation has been so far demonstrated between PTX3 and the prognosis of such diseases, or the risk associated therewith. In particular, PTX3 did not prove an independent predictor of infective-state progression in sepsis (Müiller et al., J. Leukoc. Biol. 2002; 72: 643-649). An important study has been carried out by Peri et al. (Circulation 2000; 102: 636-641) on 37 patients with acute myocardial infarction. The levels of PTX3 increased in infarcted patients, peaking at 6.94±11.26 ng/ml (mean±standard deviation) 7.5 hours after admittance at the hospital coronary units. In this study PTX3 was not associated with any risk factor, apart from patient's age.